Hull York Medical School, University of Hull, Hull, UK.
School of Life Sciences, University of Hull, Hull, UK.
J Thromb Haemost. 2017 Dec;15(12):2289-2299. doi: 10.1111/jth.13871. Epub 2017 Nov 8.
Cancer is associated with an increased risk of venous thromboembolism (VTE); the exact mechanisms for the induction of VTE remain to be fully elucidated, but it is widely acknowledged that tissue factor (TF)-bearing microparticles (TF-MPs) may play a significant role. However, TF-MPs have yet to be accepted as a genuine biomarker for cancer-associated VTE, as the presence of elevated TF-MP levels is not always accompanied by thrombosis; interestingly, in certain cases, particularly in pancreatic cancer, VTE seems to be more likely in the context of acute inflammation. Although several potential mechanisms for the development of VTE in cancer have been postulated, this review explores the homeostatic disruption of TF-MPs, as the main reservoir of bloodborne TF, in the context of cancer and inflammation, and considers the abrogated responses of the activated endothelium and mononuclear phagocyte system in mediating this disruption.
癌症与静脉血栓栓塞症（VTE）的风险增加有关；诱导 VTE的确切机制仍有待充分阐明，但广泛认为组织因子（TF）载入微颗粒（TF-MPs）可能起重要作用。然而，TF-MPs 尚未被接受为癌症相关 VTE 的真正生物标志物，因为升高的 TF-MP 水平的存在并不总是伴随着血栓形成；有趣的是，在某些情况下，特别是在胰腺癌中，VTE 在急性炎症的情况下似乎更有可能发生。尽管已经提出了癌症中 VTE 发展的几种潜在机制，但本综述探讨了 TF-MPs 的内稳态破坏，因为 TF-MPs 是血液来源 TF 的主要储库，在癌症和炎症的背景下，并考虑了激活的内皮细胞和单核吞噬细胞系统在介导这种破坏中的作用。
